methylatropine and Atrial-Fibrillation

Analysis of heart rate variability (HRV) has thus far not been applied in patients with atrial fibrillation, probably because of the presumed absence of any form of patterning of the ventricular rhythm, particularly vagally mediated respiratory arrhythmia. However, such patterning is theoretically conceivable given the function of the atrioventricular node in atrial fibrillation and its susceptibility to autonomic influences.. Sixteen patients (mean age, 56+/-4 years) with long-term atrial fibrillation on fixed doses of digoxin or verapamil were studied; 12 healthy men in sinus rhythm were used as control subjects. HRV (standard deviation of RR intervals [SD], coefficient of variance [CV], the root-mean-square of successive difference [RMSSD], and low-frequency [LF] and high-frequency power [HF]) was analyzed during 500 RR intervals at baseline, after administration of propranolol (0.2 mg/kg I.V.), and after subsequent administration of methylatropine (0.02 mg/kg I.V.). HRV at baseline and changes in HRV after methylatropine were then related to vagal tone (vagal cardiac control), quantified as the decrease in mean RR after methylatropine. Baseline HRV was higher in the atrial fibrillation group than in the control group; after propranolol, HRV increased in both groups; after methylatropine, HRV neared zero in the control group, whereas it returned to baseline values in the atrial fibrillation group. SD, RMSSD, LF, and HF at baseline were significantly (P<.05) correlated with vagal tone in the control group but also in the atrial fibrillation group (correlation coefficients of .60, .61, .57, and .64, respectively). Even stronger correlations were observed between changes in these parameters after methylatropine and vagal tone, particularly in the atrial fibrillation group (correlation coefficients of .89, .87, .72, and .90, respectively).. This study shows that HRV in patients with atrial fibrillation is related to vagal tone.

Topics: Atrial Fibrillation; Atropine Derivatives; Case-Control Studies; Female; Heart Rate; Humans; Male; Middle Aged; Parasympatholytics; Propranolol; Reference Values; Sympatholytics; Vagus Nerve

1. Animal studies suggest that the heart-rate-lowering effect of vagal stimulation during atrial fibrillation is due to: (1) a direct depressant effect on atrioventricular node conductivity, (2) enhancement of concealed atrioventricular nodal conduction of atrial impulses through augmenting fibrillatory activity, thereby indirectly prolonging atrioventricular nodal refractoriness. The purpose of the present study was to analyse these effects in man. 2. Sixteen patients with chronic atrial fibrillation were studied. After administration of propranolol (0.2 mg/kg intravenously) baseline ventricular rhythm was recorded (500 R-R intervals). Recordings were repeated after methylatropine (0.02 mg/kg intravenously). The shortest R-R interval was taken to represent atrioventricular nodal refractoriness. The ratio of the longest to the shortest R-R interval and the coefficient of variation of R-R intervals were used as parameters of concealed conduction. 3. Methylatropine foremost shortened long R-R intervals: values for the mean, shortest and longest R-R intervals decreased from 834 to 685 ms (-18%) (P < 0.001), 573 to 498 ms (-13%) (P < 0.001) and 1228 to 924 ms (-25%) (P < 0.001), respectively. Accordingly, the ratio of the longest to the shortest R-R interval decreased: 2.12 to 1.89 (-11%) (P < 0.05). Also, the coefficient of variation decreased: 0.24 to 0.20 (-17%) (P < 0.05). 4. This study supports the contention that vagal stimulation lowers ventricular rate during atrial fibrillation both by exerting a direct effect on the atrioventricular node and by augmenting concealed conduction.

Topics: Adult; Aged; Aged, 80 and over; Atrial Fibrillation; Atrioventricular Node; Atropine Derivatives; Chronic Disease; Depression, Chemical; Female; Heart Rate; Humans; Male; Middle Aged; Parasympatholytics; Vagus Nerve